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The interaction of ouabain and epinephrine on diastolic depolarization of canine Purkinje fibers was studied using conventional microelectrode techniques. When the Purkinje fibers were treated with ouabain alone, they developed slow diastolic depolarization accompanied by a proportionate decrease in the maximum diastolic potential. When these digitalized Purkinje fibers were further treated with epinephrine, the rate of these changes was greatly accelerated, resulting in rapid spontaneous activity in some Purkinje fibers. The rate of development of increased automaticity observed in the preparations treated with both ouabain and epinephrine was two to three times faster than that observed in the preparations exposed to ouabain alone. Epinephrine alone at the same concentration caused minimal changes in diastolic depolarization of these preparations. Propranolol in a beta-receptor blocking dose prevented the potentiating effect of epinephrine but did not interfere with the effect of ouabain on diastolic depolarization of Purkinje fibers. It is concluded that epinephrine potentiates the ouabain-induced increase in automaticity of Purkinje fibers by stimulating beta receptors. KEY WORDS adrenergic activity diastolic depolarization digitalis propranolol adrenergic blockade• It is well established that lethal doses of digitalis result in ventricular fibrillation in both experimental and clinical situations. Digitalis has been shown to increase idioventricular pacemaker activity in intact animals (1-3) and the slope of diastolic depolarization of Purkinje fibers in in vitro studies (4-6). Catecholamines, both norepinephrine and epinephrine, are noted for their ability to increase automaticity of Purkinje fibers. Seevers and Meek (7) have observed that ephedrine, a sympathomimetic amine, frequently results in ectopic ventricular activity when it is administered to dogs together with digitalis. Roberts et al. (8) have shown that reserpine, which depletes catecholamine stores in adrenergic nerve endings, reduces the capacity of cardiac glycosides to induce extrasystoles in dog hearts. Erlij and Mendez (9) have also found that cardiac arrest rather than ventricular fibrillation is the common terminal event in reserpinized dogs. Mendez et al. (10) and Erlij and Mendez (9) have shown that dogs subjected to cardiac denervation and adrenalectomy usually go into cardiac arrest rather than ventricular fibrillation after administration of a toxic dose of digitalis.Since sympathetic activity is constantly present in individuals and varies in degree at different times, the question of whether catecholamines contribute to the development of digitalis-induced cardiac arrhythmias arises. In the present study, microelectrode techniques were used to study the effect of epinephrine on ouabain-induced changes in automaticity of canine Purkinje fibers. MethodsHearts were excised from dogs anesthetized with sodium pentobarbital (30 mg/kg, iv). Papillary muscles with attached false tendons were dissected from the right or the left ventricle...

The canine atrioventricular (AV) junction comprises three major tissues: paranodal fibers (PNF), AV node (AVN), and His bundle (HB). In the present study, dissection-exposed, in vitro canine AV junctional preparations were used. The object of the study was to determine whether the PNF or AVN was more sensitive to the suppressive effect of acetylcholine (ACh). In five experiments these tissues were stimulated antegradely and retrogradely, and their action potentials were recorded simultaneously under the influence of ACh (0.5 micrograms/ml). Results indicated the PNF were more sensitive to the suppressive effect of ACh than were the AVN. In another group of 13 experiments, the effects of ACh at 0.05-0.3 micrograms/ml on rate of rise of phase 0 of action potentials (Vmax), peak potential, resting membrane potential, and action potential duration of the PNF were determined. Results indicated that ACh exerted a strong suppressive effect on Vmax and amplitude of the action potentials and had little effect on the resting membrane potential and action potential duration of the PNF. In 10 of 13 preparations, ACh also suppressed the response of PNF, resulting in generation of one action potential to every two stimuli. In conclusion, these findings suggest that PNF could be the tissue responsible for vagal-induced AV conduction block.

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The present study, using in vitro preparations, was designed to determine the anatomic, histological, and automatic properties of canine paranodal fibers. This tissue, together with the atrioventricular (AV) node and His bundle, constituted the three major tissues in the AV junction. The fascicles of the paranodal fibers ran parallel and adjacent to the base of the septal cusp of the tricuspid valve. The distal end of the paranodal fibers joined the lower half of the compact AV node on its convex side. Paranodal fibers when isolated were able to initiate spontaneous activity. Action potentials of many of these fibers showed primary pacemaker characteristics, i.e., a prominent phase 4 depolarization and smooth transition from phases 4 to 0. In 14 preparations, epinephrine (2.0 micrograms injected into the tissue bath) potentiated spontaneous rates to 144 +/- 6.0 beats/min from 61 +/- 5.0, an increase of 136%. Also, under the influence of epinephrine, paranodal fibers consistently generated a spontaneous rate higher than that of the AV node or His bundle, whether they were functionally connected or separated. These findings provide a basis for explaining the junctional tachycardia that occurs under adrenergic influence and demonstrate the presence of three major automatic tissues: the paranodal fibers, AV node, and His bundle in the canine AV junction.

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